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117 Cards in this Set

  • Front
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AE for magnesium IVP for torsades (what is going to happen if you give it fast)
it's going to cause bradycardia- stop HR
class Ia drugs-effect on heart (2) usage
Decrease conduction velocity and increase action potential duration

Used most frequently for conversion of atrial flutter/fibrillation and maintenance of sinus rhythm
class Ib drugs- effect on heart (2)

usage (2)
Minimal change in conduction velocity and slight decrease in action potential duration

Not useful for atrial arrhythmias

Used for ventricular arrhythmias, especially those associated w/MI (but not for prophylaxis)
Class Ic drugs- effect on heart

usage
Marked prolongation of conduction velocity- proarrhythmic

Used for atrial flutter/fibrillation in patients w/structurally normal hearts
Class Ia drugs- MoA - channel fx (2)
block Na+ intermediate on/off rate-
and K+ channels
Class Ib drugs- channel fx
Na+ fast on/off rate
Class Ic drugs- channel fx
Na+ slow on/off rate
class II drugs
block what
beta blockers
Ca+ channels...(indirect?)
Class III drugs- target
example
K+ channel
amiodarone, sotalol, dofetilide
Class IV drugs
non DHP CCBs
Class III drugs- effect on heart
usage
prolong action potential duration

used in both atrial and ventricular arr.
mnemonic for classes of antiarrhythmics
N (sodium) O (I)
Boys (beta blockers) (II)
Kiss (K+) (III)
Carrie (Ca++) (IV)
Omissions from Vaughan Williams (2)
adenosine
dig
adenosine pearls- what drugs will affect it (DDI) (2)

and hypersensitivity?
Potentiated by dipyridamole (adenosine uptake inhibitor)

Inhibited by methylxanthines (block receptor)- if on gout shit have to give more adenosine

Hypersensitivity in cardiac transplant (cut vagal nerve) patients can cause asystole
Type Ia drugs (3)
Quinidine
Procainamide
Disopyramide
3 characteristics of Ia drugs (moa)
Moderate Na+ channel blocking
Decreased conduction velocity
Prolonged repolarization
extra effects of quinidine (2)
α-adrenergic block and vagolytic
quinidine (other targets than Na+) (2)
α-adrenergic block and vagolytic
what happens if you give quinidine alone, or IV?
HoTN (hypotension) when given IV
Acceleration in AV conduction if used alone (must combine w/ß-blocker)
quinidine metabolism (2 proteins)

implication?
Hepatic metabolism- CYP2D6 and PgP (raises dig lvls- i guess more so with pgp)
quinidine dosing IR and SR
IR q6h- start with this, and convert to SR
SR q8-12h
7 AEs of quinidine
N/V/Diarrhea 25-50%
Cinchonism- variety of AE (tinnitus, vertigo, blurred vision...)
Bone marrow suppression
Reversible thrombocytopenia
Hemolytic anemia
Hepatitis
Lupus-like syndrome (drug fever)
Least anticholinergic of Ia class
quinidine
procainamide AE/tolerance (2)
Better tolerated IV than quinidine
BUT
70% get anti-nuclear antibodies, especially slow acetylators
resulting in Lupus-like syndrome (30% of long-term users)
you can go down from loading dose of procainamide early if...(3)
QRS widens > 50%, significant HoTN, or arrhythmia abolished
disopyramide usage (2)
Rarely used except for hypertrophic cardiomyopathy and neurocardiogenic syncope
disopyramide effect on heart
very negative inotropic effect
Class I antiarrhythmics- avoid in what condition
HF!!!
disopyramide AE (why it isn't used) (3)
Prominent anticholinergic effects (dry mouth, urinary retention, constipation, blurred vision)
N/V
Hepatic cholestasis
disopyramide metabolism
CYP3A4
Type Ib drugs (2)
Lidocaine
Mexiletine
characteristics of Ib drugs (3)
Mild Na+ channel blocking
Shortened repolarization
Slight decrease in conduction velocity
lidocaine route- why?
Given IV d/t hepatic first-pass metabolism
dosing of lidocaine- adjustments? (2)
decreases dose in liver and heart failure
lidocaine- metabolism effects/monitoring
inhibits it's own metabolism- so in hospital you have to get daily level of the drug (level will increase)
AE for lidocaine (3)
Neurologic (paresthesias around mouth, sedation d/t accumulation of MGX metabolite in renal failure, tremor, nystagmus, delirium, seizures)
Less GI toxicity relative to mexiletine
AV block
lidocaine metabolism enzymes (2)
CYP3A4 and 2D6 substrate
mexilitene- what is it
metabolism route
PO equivalent to lidocaine
Hepatic metabolism
mexiletine AE (2)
GI (take w/food), occasionally CNS
other...besides lidocaine...infrequently used Ib drugs (2)
Phenytoin
tocainide
tocainide AE (2)
bone marrow suppression, pulmonary fibrosis
Ic drugs (2)
Flecainide
Propafenone
Ic drug properties (3)
Significant Na+ channel blocking
Decreased conduction velocity
No effect on repolarization
Flecainide- what is it
usage (3)
Minor K+-channel blocker
Occasionally used in AVNRT (nodal re-entrant tachy) or Afib

mostly used for vt
flecainide mortality rates- when/why
Increased mortality after MI in CAST (can cause monomorphic VT)
3 categories for AE in flecainide
cardiac
CNS
GI
flecainide metabolic enzyme
CYP2D6 substrate
cardiac AE for flecainide (3)
Cardiac: AV block, HF, proarrhythmic
CNS AE for flecainide (3)
CNS: dizziness, headache, blurry vision
GI/mouth AE for flecainide (2)
GI: dysgeusia (metallic taste), N/V
propafenone- additional activity
S-enantiomer is ß-blocker
propafenone- metabolism (3)
Substrate of CYP2D6, 3A4, and 1A2
selective metabolite of propafenone and what it targets
5-OH propafenone blocks Na+ channels but not ß receptors
propfenone DDIs (3)
Increases digoxin (~ 80%), warfarin, metoprolol
propafenone- renal/hepatic disease dosing
Renal and hepatic dose adjustments...
propafenone cardiac AE (30
Cardiac: QTc prolongation, AV block, HF
propafenone GI AE (3)
metallic taste, dry mouth, constipation
moricizine (2) what is it
use?
Phenothiazine derivative
Increased mortality after MI in CAST-II so not used
only class of drugs that reduce mortality in arr.
class II (BBs)
beta blockers (class II) effect on heart (4)
Lowers sinus conduction rate
-Decreased conduction velocity
-Increased refractory period

Prolong action potential and slow heart rate
6 AE for BBs
HF
Depression
Bronchospasm
Impotence
Fatigue
AV block
Class III drugs (4)
Amiodarone
Dofetilide
Ibutilide
Sotalol (d-isomer)
Type III drug effects on heart (2)
Significant K+ channel blocking
Prolongation of refractory period
amiodarone- drug properties
MoA (principal)
Broad spectrum class III agent w/effects in all 4 Vaughn-Williams classes
Principal MOA = delaying repolarization
amiodarone usage (2)
Safe in both atrial and ventricular arrhythmias
amiodarone- 8 categories of AE
cardiac
pulmonary
thyroid
ocular
neuro
derm
hepatic
GI
amiodarone cardiac AEs (2)
HF (usually well tolerated in these patients)- because of BB property- but still the only drug other than dofentilinide that can be used in HF
Torsades (< 1% due to QT prolongation, but less than other class III agents)
pulmonary AE for amiodarone
3% of patients may get pulmonary fibrosis or delayed hypersensitivity pneumonitis

ergo Patient MUST report unexplained dyspnea, cough, or fever
half life of amiodarone
58 days...
thyroid AE of amiodarone (2) why?
do you treat?
44% of drug is iodine
Hypo- or hyperthyroidism

do not give treatment of subclinical hypothyroidism!
ocular AE for amiodarone- main one

when this becomes and issue

monitoring
Corneal deposits occur in nearly all patients so treatment needed

only issue if they get Halos, photophobia, and overt retinopathy may occur

Eye exam (w/slit lamp) yearly
neuro AE of amiodarone (3)
Tremor, ataxia, peripheral neuropathy in 20-40% of patients (tremor not uncommon w/long-term therapy)
derm AE of amiodarone (2)
sun exposed skin = blue tinge (smurfing)
Photosensitivity! use sunscreen
hepatic AE of amiodarone (2)

hepatitis?

monitoring
Asymptomatic transaminitis and hyperbilirubinemia in 4-25%

Rarely hepatitis so just monitor

LFTs q6months
GI AE of amiodarone (3)
N/V (mostly with loading doses)
Loss of taste
Constipation
DDIs of amiodarone (major ones)
(5 drugs)

HUNDREDS of DDIs
digoxin
warfarin
Increases levels of BBs, phenytoin, theophylline
dig/warfarin + amiodarone- how to handle (2)
dig- empirically reduce dose by 50%
warfarin- reduce dose by 30%
8 monitoring things for amiodarone fuck
CXR, EKG q3-6months (fibrosis)
Thyroid (S/sx hypothyroidism), LFTs q6months
Annual eye exam
Continuous dry cough ± dyspnea
Nausea should diminish with time
Photosensitivity
dronederone- SAR (3)
amiodarone relative

removed iodines to lower thyroid issues
methylsulfonamide group to reduce lipophilicity and reduce neurotoxic fx

BA sucks
dronedarone fx on SCr
elevates SCr but doesn't affect renal fxn
dronedarone half life
16 h much much shorter than amiodarone
dronedarone HUGE CI ****
dronederone- big issue- CONTRAINDICATED IN HF ( i guess decompensated was the one that was studied)

so...just...use amiodarone
dronederone- metabolism/DDIs

interacts with what 2 proteins

which drugs? (2)

what drug does it not interact with, that amiodarone does?
Metabolized by CYP3A4/competes for PgP

drug interactions: ketoconazole increases AUC 15 fold
Digoxin increases by 2.5x- due to pgp competition

No warfarin interaction (amiodarone does)
in pt with persistent AF- amiodarone vs. dronederone

results
cardioversion -->then dronederone or amiodarone

AF recurrence was higher in dronedarone but fewer ADRs with drone- less effective

less adherence with amiodarone
Contraindications for dronederone (2)

not studied in what pop
HF (IV, and II-III if decompensated, within last month)

Qt prolongation

not studied in hepatic/pregnancy

Not studied in hepatic or pregnant women
AE for dronederone (4)
GI/bradycardia/QT prolongation/SCr increase
indications for dofetilide
Conversion and maintenance of AF (only atrial arr.) to NSR
AE of dofetilide (4)
Cardiac: 3-6% risk of Torsades
CNS: headache, dizziness
Chest pain
2 DDIs with dofetilide (out of a million)
hctz, bactrim
2 antiarr. safe to use in HF
dofetilide
amiodarone
dofetilide CI (1 CI, 1 other)
Contraindicated if QTc > 500 msec
must be hospitalized for 3 days
dofetilide metabolism
CYP3A4 substrate
risk for torsades with dofetilide increases with...(3)
Risk increases w/renal insufficiency, prolonged baseline QTc, other QTc prolonging drugs (fluconazole, haloperidol, fluoroquinolone)
ibutilide- main AE

when will this AE occur? (2)
2-5% incidence of Torsades

most likely will occur within first 24 h
or pt with HF
ibutilide DDI
none
ibutilide monitoring
Continuous EKG monitoring for first 4 hours of infusion
sotalol- properties (4)

what is it
potency as a BB
2 others
BB w/class III properties
Not that potent of BB
Minimal effect on PR intervals- idk why
Proarrhythmic
sotalol- which eniantomer is antiarrhythmic?
Only d-sotalol is antiarrhythmic
sotalol- "place" and therapy
Typically second-line after amiodarone- better for younger pt (due to AE of amiodarone)
8 sotalol ADRs
Dose-dependent increase in QTc interval (and torsades)
AV block
HoTN
HF
Bronchospasm
Depression
Fatigue
Impotence
when would you d/c sotalol due to QTc interval prolongation
>520
sotalol + other BB for rate control? is this ok?
yes- for rate control it's ok because sotalol is so weak
5 characteristics/effects on heart of type IV antiarrhythmics
Calcium channel blocking
Decreased sinus rate
Slow conduction
Prolong refractoriness
Decrease automaticity
Type IV (CCB)- usefulness/indication (2)
Useful for controlling ventricular response in AF
exercise-related tachycardias
verapamil/diltiazem ADR (5)
GI: constipation**worse in verapamil, anorexia, nausea
Peripheral edema
Hypotension
verapamil enzymes/proteins it interacts with (3)
CYP3A4 and 1A2 substrate
CYP3A4 inhibitor
P-glycoprotein inhibitor
CCBs in CHF
neg inotropic effect limits use in HF- though diltiazem has less (can see it sometimes if stable HF)
diltiazem DDIs (2)
CYP3A4 substrate and inhibitor
P-glycoprotein inhibitor
digoxin uses (2)
Atrial fibrillation with RVR (negative chronotrope)
Heart failure for morbidity benefit only (positive inotrope)
digoxin- dosing- use what weight?
Does not distribute into adipose tissue → IBW
half life of digoxin
elimination route?
Half-life at steady-state = 36 h (24-46 h)
mostly renal: only 15% of digoxin is eliminated non-renally
therapeutic range for HF vs AF for digoxin
1-2 mcg/mL for AF
0.5-1 mcg/mL for HF
3 major DDIs with dig
quinidine
amiodarone
verapamil
verapamil + dig- how to alter dig dose
Decrease dose by 25% if concomitant verapamil
quinidine/amiodarone + dig- how to alter dig dose
Halve dose if concomitant quinidine and amiodarone
disease state interactions and what to do with dose- digoxin (4)
Reduce dose for untreated hypothyroidism
increase dose if untreated hyperthyroidism
Reduce in renal failure
Reduce in HF
digoxin toxicity sx (5)
Fatigue
confusion/agitation/hallucinations
GI: N/V/D
Visual symptoms (halos)
CV- anything you can think of
(think of van gogh)